Monitoring the Redox Status in Multiple Sclerosis

Abstract

Worldwide, over 2.2 million people are suffered from multiple sclerosis (MS), a multifactorial demyelinating disease of the central nervous system, characterized by multifocal inflammatory or demyelinating attacks associated with neuroinflammation and neurodegeneration. The blood, cerebrospinal fluid, and postmortem brain samples of MS patients evidenced the presence of reduction-oxidation (redox) homeostasis disturbance such as the alternations of oxidative and antioxidative enzyme activities and the presence of degradation products. This review article discussed the components of redox homeostasis including reactive chemical species, oxidative enzymes, antioxidative enzymes, and degradation products. The reactive chemical species covered frequently discussed reactive oxygen/nitrogen species, rarely featured reactive chemicals such as sulfur, carbonyls, halogens, selenium, and nucleophilic species that potentially act as reductive as well as pro-oxidative stressors. The antioxidative enzyme systems covered the nuclear factor erythroid-2-related factor 2 (NRF2)-Kelch-like ECH-associated protein 1 (KEAP1) signaling pathway, a possible biomarker sensitive to the initial phase of oxidative stress. Altered components of the redox homeostasis in MS were discussed, some of which turned to be MS subtype- or treatment-specific and thus potentially become diagnostic, prognostic, predictive, and/or therapeutic biomarkers. Finally, monitoring a battery of redox components including oxidative, antioxidative and degradation products helps evaluate the redox status of MS patients, which expedites prolongation of remission, relapse prevention, and building personalized treatment plans.

Single Nucleotide Polymorphisms of Indoleamine 2,3-Dioxygenase Influenced the Age Onset of Parkinson’s Disease

“…miR-133b, miR-7, miR153, miR-433, miR-433, miR-205, and miR-124 are of interest as possible biomarkers in PD [55]. Furthermore, differential monitoring of the redox status was proposed to build a personalized treatment for patients with multifactorial neurologic diseases [56] This study had several limitations including its relatively small sample size, the small number of SNP loci, heterogeneity of the study subjects, and the collection of blood samples at a single center. Furthermore, enzyme activities of IDO1, IDO2, and TDO were not measured.…”

Antioxidant Therapeutics in Parkinson’s Disease: Current Challenges and Opportunities

“…Oxidative stress affects cellular function by targeting nucleic acids, lipids, and proteins, all of which are constituents of cell organelles [ 23 ]. RS comprises not only ROS, and reactive nitrogen species (RNS), but also reactive sulfur species (RSN), reactive carbonyl species (RCS), reactive halogen species (RHS), reactive selenium species (RSeS), and reactive nucleophilic species [ 24 ], generated by biological processes within the cell in normal and stressful conditions. Biomolecules are highly susceptible to oxidation by one or more ROS and RNS present in the environment, generated as by-products of normal metabolism, or during exposure to X, λ, or UV irradiation.…”

Co-Players in Chronic Pain: Neuroinflammation and the Tryptophan-Kynurenine Metabolic Pathway

“…Disturbance of KYN metabolites has been linked to immune disorders, cancers, neurodegenerative diseases, and psychiatric disorders [27]. Furthermore, TRP-KYN metabolites are under extensive research in search of peripheral biomarkers as well as novel drug prototypes for a wide range of diseases [28][29][30][31][32][33][34]. Inflammation activates the TRP-KYN pathway, elevating the levels of oxidative compounds or neurotoxic ligands to receptors of the excitatory glutamatergic nervous system, which damage the peripheral nervous system or CNS through the broken blood-nerve or blood-brain-barrier, respectively [16].…”